WHAT THE CORONER SAID - PowerPoint Presentation

1. WHAT THE CORONER SAIDtake 2“To err is human” Dr E HolbeachHMO supervisorApril 2017

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3. CASE 1

4. 66 yo maleTravelling to visit family in AustraliaPHx:IHDArthritisMeds‘bought from local market in home town’HOPC: ran out of usual meds. Arthritis pain worsened- attended hospital. Referred to Medical Clinic (GP) for review

5. Seen by locum GP Dr HDaughter acted as interpreterCommenced on: Methotrexate: 5mg/d for 5 daysThen increase to 10mg/d for 7 daysRegular Anti-inflammatoriesIMI corticosteroidGP hand wrote a letter for patient to take home to own country:“methotrexate 10mg preventer. Start with ½ tab once a day, do this for 5 days then 1 tablet once a day x 1 week. May need to increase twice a day = Check kidney ->1/12 full blood exams”

6. Mr L’s family went to pharmacy there was delay in having script filled.Mr L’s family then showed pharmacist the handwritten note, after which the methotrexate was dispensed as prescribed.Label on the bottle “No directions specified, please check with prescriber if unsure of usage”Pharmacist gave family a printout information sheet about methotrexate and informed them that usual dosing is weekly not daily.

7. Progress:Commenced methotrexateInitial improvement in symptomsThen: stomach pains, vomiting, excessive urinationReviewed by same GP: UTI diagnosed antibiotics and antiemeticsDiarrhoea worsenedMouth ulcersSelf-ceased methotrexate (after taking 4days of 5mg/d dose)9 days post onset GI symptoms presented to EDPancytopeniaSepticaemiaARICoagulopathyLow albuminXRAY: SBO, stoghorn calculus r kidney, apical lung lesion ?prior TBDiagnosis?Transferred to major metro hospital

8. Progress:Protracted and stormy over monthsMultiple admissions to ICUFBE normalised, but:GI bleeding– laparotomy/ gastroscopiesSepsisWorsening renal failure- right kidney removedReactivation of TBDeceased in hospital 4months after starting methotrexate

9. Post Mortem: multiple organ failure associated with the combined effects of methotrexate toxicity, vasculitis, atherosclerotic cardiovascular diseaseInvestigation:What would you want to know as a the coroner? Two key questions….1. What role did methotrexate have in the cause of death2. Responsibilities of doctors and dispensing pharmacists.Coroner’s findings?

10. What the Coroner said:

11. So what were the errors here?Knowledge base?Authority and Hierarchical Error?

12. Medication Errors:VERY VERY VERY Common cause of Iatrogenic Adverse Events….Most of the errors are NOT knowledge base… BUT beware….A- PINCH meds:Anti-infectivesPotassiumInsulinNarcoticsChemotherapeuticsHeparin and anticoagulants

13. MethotrexateInhibits dihydrofolate reductase which reduces folic acid to tetrahydrofolic acidOld drug- one of the first chemo drugs around. Has been used for rheumatological conditions since 1960sToxic Effects:Minor: stomatitis, malaise, nausea, diarrhea, headaches and mild alopeciaMajor: hepatic, pulmonary, renal and bone marrow abnormalities- suppression, lymphomaPrevention of toxicityFolate supplementationBoth men and Women should use contraception whilst on MTX therapyMTX Toxicity treatment: -leucovorin (folinic acid) (reduced and active form of folic acid-others to consider: thymidine, glucarapidase (avail in australia?!)Special cases: Intrathecal overdose: CSF fluid drainage!!! exchange, steroids, antidotes

14. Authority and Hierarchical ErrorsWhat is this?How does it come into effect in this case?Aviation Industry well describes this errorPoorly researched in Health careDo you think it’s an issue in Health Care?Who is to responsible: The top of the chain, or the bottom?How to overcome?Checklists, cross-checks, read-backs, graded assertiveness and rules that support the ability to challenge our senior colleagues

15. CASE 2

16. Mrs F admitted for lap R hemicolectomy for removal of caecal polypSurgery uneventful2days post-op: abdo distensionIleus/ SBONGT insertedSome improvementDay 10 of fasting decision to start TPNPICC inserted under image intensifier in radiologyThat night: New AFHypokalaemiaNext two days- closely monitoredLarge NGT lossesTPN rate increased from 20mL/hr 60mL/hr 2 days later: deteriorated rapidly, ICU treatment, died.

17. Pathology/ Post Mortem: Any guesses as to what happened?Report:Distended small and large bowel, but anastomosis intactNo findings to explain ileus/ obstruction300mL of white milky fluid in the pericardiumEvidence of perforation of right ventricular wallCause of death?Cardiac Tamponade as a consequence of a ruptured heart as a consequence of total parenteral nutrition

18. InvestigationHow and when the right ventricle was perforatedWhether cardiac tamponade should have been identifiedCoroner’s FindingCoroner accepted that the risks are rare but known, and was unable to make any recommendations to avoid similar deaths in the future

19. CASE 3

20. Mr G, 63 yo, admitted to local hospital for emergency right hemicolectomy due to necrotic bowelPast hx: COPD, ETOH addiction, bipolar affective d’o, CRI, CLD with cirrhosisPost op- HDU given comorbiditiesETOH withdrawal scale- administered benzodiazepines over 24hrsDay 2 post op: nurse worried about resp compromise. Reviewed by surgeon: “ keep in mind he smokes 60ciggs/day and will surely be a CO2 retainer so be careful how much O2 you give him”If SpO2<85% or RR>30- to commence BiPAPAlso developed hypernatraemia-> N/S changed to dextrose

21. Progress:Deteriorated Commenced BiPAPBecame unresponsive shortly after starting biPAPMET- intubated, ventilatedWorking diagnosis for deterioration: CO2 narcosis or hypernatraemiaDr T (anaesthetist) reviewed patient- decision with Mr G (surg) was for transfer to tertiary centre for ICUCVC inserted, CXR requestedTransferred to Tertiary hospital: repeat CXR to check ETT and CVC line positionDay 2 ICU- nurse checked CVP via CVC transducer. Results suggested CVC arterially placed- ABG taken, confirmed this.All infusions stopped patient had received: insulin, glucose, propofol, vitamin K and pantoprazole via arterially positioned CVCDay3: CTB: large right hemisphere infarct.Thought to be secondary to all the medications being delivered directly to the brain via carotid artery. Deemed catastrophic and irreversible. Palliative care approach- died (?weeks later)

22. Cause of death:Brain injury caused by inadvertent misplacement of the central line into the carotid arteryCoronial Investigation:What would you want to know?Findings:Checking measures were not mandated at the initial hospital when Mr G was admitted.A state-wide (NSW) policy was brought in to require clinicians to complete written confirmation of CVC placement and site confirmation

23. LINES!!What’s a PICC?What’s a CVC?

24. PICC insertionMust have consent- single or double lumenINR<1.5Lots of documentation required!Daily measurement of length

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28. CVPsWhat’s a normal CVP? (2-6mmHg)How to measure? (lying flat, end expiratory)Insertion?How to tell if it’s in the right place?Not by pulsitilityNot by blood colourNot by ABGUSE TRANSDUCER!

29. Complications of central venous access:InfectionThrombosisEmboliArrhythmiaCardiac or Vascular injuryInadvertent infusion toxicity (intra-arterial or extravascular)PneumothoraxRetained guide wiresMost can be reduced by use of real time ultrasound during insertion

30. Cases at Northern?

31. CASE 4

32. Mr SB 38yo maleSeen by GP for referral letter to resp physicianPHx:Bipolar affective d’oAsthmaITPBMI 30Smoker6months of breathlessness, worse over last one weekLeft sided pleuritic chest painFebrile, tachypnoeic, tachycardic SpO2 96% RA and reduced AE to left lung baseGP referred to ED!

33. 16:30(2 hrs later) presented to ED:ED Triage: BP 110/48, HR 132, RR 28, Temp37.9, SpO2 96%16:34: Seen by HMO 16:50: Discussed with senior medical officer16:55: Moved to rescusO2 via hudson maskIV TAntibioticsCXR: consolidation and pulmonary congestionECG: sinus tachycardia, left axis deviation

34. 17:30 confused, diaphoretic and agitatedSeen by ED consultant: cold mottled skin, febrile, HR150, RR 30 SpO288%Commenced NIV whilst set up for intubationDifficult intubation due to fluid in airway. Tubed at 18:3018:34 arrest with EMDCPR for 70minutesBedside echo: no contractility of the heartDeceased 19:55Working diagnosis:Toxins/ drugsAtypical infectionsPreexisting cardiomyopathy

35. Pathology/ Post mortem:Thoughts?PE and lung infarctsBilateral calf DVTDilated cardiomyopathyMild obesityPulmonary oedemaInvestigation:Staff involved, independent expert statements from forensic medicine clinician, intensivist, professor of emergency medicineMr SBs family engaged two further independent experts: emergency medicine physician and a vascular surgeon

36. Vasc Surg and and ED physician engaged by family: PE should have been among initial diagnosis, ECG gave strong clues to this, and that CTPA should have been arranged and thrombolysis would have prevented death.Forensic Medicine expert: more circumspect. ECG changes non specific. Thrombolysis may not have changed outcome. Also felt that it was reasonable that Mr SB was not treated for a PE prior to cardiac arrest when a team of x3 ED doctors, x2 intensivists and x1 cardiologist all thought pneumonia most likelyIntensivist: agreed with Forensic Medicine expert. Also pointed out that PE prediction tool had Mr SB as not a high risk when he presented.Prof of Emerg Med. Agreed calculated risk for PE was low and that pneumonia was appropriate working diagnosis. Also discussed that thrombolysis was not indicated in the setting of an undifferentiated cardiac arrest. Agreed that PE should have been considered, but felt that any pathology or imaging would not have been available in time to change course of events.

37. Coroner’s findings?Felt that exploring difference of opinions around whether correct diagnosis should have been established or whether thrombolysis would have prevented death were unlikely to bring about any useful recommendations to improve patient safety

38. CASE 5

39. Mr SM 32 yo obese man with intellectual disabilityRecent ankle injuryAdmitted with acute appendicitis and peritonitisEmergency surgery- returned to ward just before midnight on low flow O2Early hours of the morning: tachycardic, hypotensive. Calves soft non tenderD1 post op: showered himself, sitting in chair. Needed encouragement to mobiliseSats85% RA, required mask for sats of 97%Was on Ortho ward, not General Surgical ward. So reviews over next few days more ad-hocD3: abdo pain and distension. Diagnosed with paralytic ileus. NGT insertedOngoing periods of hypoxia 78-80% when he pulled off maskD4-5: Commenced on treatment for aspiration pneumonia after review by surgeonPain levels improved, bowel function improvedO2 requirements decreased- now on low-flow O2D6:Complained of dizzyness while mobilising to toilet. Sat on chair, became unresponsiveCPR- unable to be revived.

40. Pathology/ Post Mortem?Large saddle embolus from DVT in right calfMicroscopic examination revealed that the thrombi a few days oldInvestigation:What would you want to know?What would you find?- fault?Whilst appropriate DVT prophylaxis was in place, management of post op hypoxia was lacking. He did not think CXR was consistent with asp pneumonia and felt ABG and other investigation could have made earlier diagnosis and changed outcome

41. Risk Prediction Tool?WELLS or Revised GENEVA scoreLow-risk group: 3-10% rateBUT: 25% of all VTEs are diagnosed in this group(note that 50-70% of patients assessed for VTE are considered low risk)Intermediate risk: 15-30% rateBUT: constitute 50% of VTE cases(note: 30-40% of patients assessed for VTE are considered intermediate risk)High risk: 40-70% rateBUT: only constitute 5-15% of cases(note: only 20-30% of patients assessed for VTE are considered high risk)PE!!

42. 2015 PE guidelines Americal College of Physicians:Use either the Wells or Geneva rules to choose tests based on a patient's risk for pulmonary embolism.If the patient is at low risk, clinicians should use the eight PERC; if a patient meets all eight criteria, the risks of testing are greater than the risk for embolism, and no testing is needed. For patients at intermediate risk, or for those at low risk who do not meet all of the rule-out criteria, use a high-sensitivity plasma D-dimer test as the initial test. In patients older than 50 years, use an age-adjusted threshold: age × 10 ng/mL, rather than a blanket 500 ng/mL (normal D-dimer levels increase with age)Patients with a D-dimer level below the age-adjusted cutoff should not receive any imaging studies. Patients with elevated D-dimer levels should then receive imaging. Patients at high risk should skip the D-dimer test and proceed to CT pulmonary angiography, because a negative D-dimer test will not eliminate the need for imaging in these patients. Clinicians should only obtain ventilation-perfusion scans in patients with a contraindication to CT pulmonary angiography or if CT pulmonary angiography is unavailable.

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44. Other issues in this case?Clinical Handover?Outliers?Intellectual disability impacting medical attention?

45. CASE 6

46. RS 2 yo boyTaken to GP for general unwellness and cervical lymphadenopathyPresumptive diagnosis: mumpsOver next 3 days: worsening malaise, LOA, abdo painTaken to ED (regional hospital)- thought to have intra-abdominal intussusception. Xrays and bloods taken – NADTransferred to regional base hospital via helicopterAt base: febrile 38.7, HR 162 (high), RR28 (high) and in painGiven opioid analgesia in ED prior to transfer to paeds wardWorking diagnosis:Intussusception was now considered unlikely (clinical picture and age)Signs of Meningism present- LP plannedLP- NADViral infection

47. That night:Ongoing irritabilityInconsolable pain- not relieved by simple non-opioid analgesia- n.staff and family concerned by pain ++Following morning:HMO suggested adding morphine to analgesia regime, septic work up, commence empirical antibiotics and IVTConsultant paediatrician disagreedPlan- AXR NADThrough the morning:RS Increasingly distressedIV cannula inserted several hrs later: b.cult/ FBE/UEC/ CRP taken

48. Results:CRP444Second paediatrician consulted late afternoon (phone)- broad spectrum antibiotics commencedSurgical reviewSurg team- suggested exploratory laparotomy that eveningAnaesthetic pre-op review- recognition that RS critically unwell and needed urgent transfer to tertiary referral centreRetrieval team- RS intubated for transferRS arrested on intubation, unable to be rescusitated

49. Pathology/ Post mortemSmall intestinal volvulus, no infarction (?agonal event)Severe bronchopneumoniaCervical and abdominal lymphadenopathyBcult results: GrpA StrepCause of death: Streptococcal Toxic ShockCoronial Investigation.?what would you find

50. Group A Strep Toxic ShockInitial presentation can mimic a range of infections and non-infectious conditionsPain often a key feature (a really really rapidly progressive painful cellulitis- think GrpA Strep)Early antibiotics crucialSepsis:Every hour of delay to antibiotics increases mortality by 7%STEP ON SEPSIS!!!!!!Antibiotics WITHIN ONE HOUR--- and YOU need to make sure they are given…. Even if it means you go to the drug room yourself….

51. But what else went wrong here?Why wasn’t it picked up?

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57. Survival TIPSKeep an open mind ALWAYS to the diagnosis.Do NOT ignore things that don’t add upESCALATE early transfer the responsibility to a consultant- call! Challenge your bosses. And when you are a boss, encourage being challenged!DOCUMENT EVERYTHING!If there is an adverse event, it is perfectly acceptable to document retrospectively- and the closer to the time it happened, the better. However, it won’t be considered as reliable as real-time documentation.Sign up to the Clinical Communique newsletters from coroners office!